Ilona Csizmadi

Adaptation and evaluation of the National Cancer Institute's Diet History Questionnaire and nutrient database for Canadian populations.

BACKGROUND AND OBJECTIVE Despite assumed similarities in Canadian and US dietary habits, some differences in food availability and nutrient fortification exist. Food-frequency questionnaires designed for the USA may therefore not provide the most accurate estimates of dietary intake in Canadian populations. Hence, we undertook to evaluate and modify the National Cancer Institutes Diet History Questionnaire (DHQ) and nutrient database. METHODS Of the foods queried on the DHQ, those most likely to differ in nutrient composition were identified. Where possible these foods were matched to comparable foods in the Canadian Nutrient File. Nutrient values were examined and modified to reflect the Canadian content of minerals (calcium, iron, zinc) and vitamins (A, C, D, thiamin, riboflavin, niacin, B6, folate and B12). DHQs completed by 13 181 Alberta Cohort Study participants aged 35-69 years were analysed to estimate nutrient intakes using the original US and modified versions of the DHQ databases. Misclassification of intake for meeting the Dietary Reference Intake (DRI) was determined following analysis with the US nutrient database. RESULTS Twenty-five per cent of 2411 foods deemed most likely to differ in nutrient profile were subsequently modified for folate, 11% for vitamin D, 10% for calcium and riboflavin, and between 7 and 10% for the remaining nutrients of interest. Misclassification with respect to meeting the DRI varied but was highest for folate (7%) and vitamin A (7%) among men, and for vitamin D (7%) among women over 50 years of age. CONCLUSION Errors in nutrient intake estimates owing to differences in food fortification between the USA and Canada can be reduced in Canadian populations by using nutrient databases that reflect Canadian fortification practices.

Case–Control Study of the Metabolic Syndrome and Metabolic Risk Factors for Endometrial Cancer

Background: Metabolic syndrome may predict endometrial cancer risk better than diabetes, hypertension, dyslipidemia, dysglycemia, or weight alone, but few studies have examined this issue. Methods: We conducted a population-based case–control study in Alberta, Canada (2002–2006) that included 515 incident endometrial cancer cases and 962 frequency age-matched controls. Data were collected through in-person interviews, anthropometric measurements, and 8-hour fasting bloods drawn either pre- or postsurgery. Bloods were analyzed using quantitative colorimetric or absorbance-based assays (ELISA), specific to metabolic syndrome markers. Metabolic syndrome was defined using harmonized guidelines requiring presence of ≥3 of the following risk factors: waist circumference ≥88 cm, triglycerides ≥150 mg/dL, high-density lipoprotein cholesterol <50 mg/dL, treatment of previously diagnosed hypertension, and fasting blood glucose ≥100 mg/dL. OR and 95% CIs for endometrial cancer risk with presence of metabolic syndrome and individual metabolic syndrome components were estimated using logistic regression analysis. Results: Metabolic syndrome was significantly more prevalent among cases (62%) than controls (38%). A statistically significant increased risk for endometrial cancer was observed for metabolic syndrome (OR = 1.53; 95% CI: 1.17–2.00), as well as for some of the individual components of metabolic syndrome including waist circumference ≥88 cm (OR = 1.57; 95% CI: 1.18–2.08), hypertension (OR = 1.57; 95% CI: 1.18–2.09), and fasting blood glucose ≥100 mg/dL (OR = 1.31; 95% CI: 1.03–1.67). Some evidence for effect modification by menopausal status and body mass index was also found. Conclusion: Metabolic syndrome is clearly associated with increased endometrial cancer risk. Impact: Targeting the entire metabolic syndrome may optimize endometrial cancer risk reduction. Cancer Epidemiol Biomarkers Prev; 20(11); 2384–95. ©2011 AACR.

Hours spent and energy expended in physical activity domains: Results from The Tomorrow Project cohort in Alberta, Canada

BackgroundKnowledge of adult activity patterns across domains of physical activity is essential for the planning of population-based strategies that will increase overall energy expenditure and reduce the risk of obesity and related chronic diseases. We describe domain-specific hours of activity and energy expended among participants in a prospective cohort in Alberta, Canada.MethodsThe Past Year Total Physical Activity Questionnaire was completed by 15,591 Tomorrow Project® participants, between 2001 and 2005 detailing physical activity type, duration, frequency and intensity. Domain-specific hours of activity and activity-related energy expenditure, expressed as a percent of total energy expenditure (TEE) (Mean (SD); Median (IQR)) are reported across inactive (<1.4), low active (1.4 to 1.59), active (1.6 to 1.89) and very active (≥ 1.9) Physical Activity Level (PAL = TEE:REE) categories.ResultsIn very active women and amongst all men except those classified as inactive, activity-related energy expenditure comprised primarily occupational activity. Amongst inactive men and women in active, low active and inactive groups, activity-related energy expenditure from household activity was comparable to, or exceeded that for occupational activity. Leisure-time activity-related energy expenditure decreased with decreasing PAL categories; however, even amongst the most active men and women it accounted for less than 10 percent of TEE. When stratified by employment status, leisure-time activity-related energy expenditure was greatest for retired men [mean (SD): 10.8 (8.5) percent of TEE], compared with those who were fully employed, employed part-time or not employed. Transportation-related activity was negligible across all categories of PAL and employment status.ConclusionFor the inactive portion of this population, active non-leisure activities, specifically in the transportation and occupational domains, need to be considered for inclusion in daily routines as a means of increasing population-wide activity levels. Environmental and policy changes to promote active transport and workplace initiatives could increase overall daily energy expenditure through reducing prolonged sitting time.

Case-control study of markers of insulin resistance and endometrial cancer risk.

Markers of insulin resistance such as the adiponectin:leptin ratio (A:L) and the homeostasis model assessment ratio (HOMA-IR) are associated with obesity and hyperinsulinemia, both established risk factors for endometrial cancer, and may therefore be informative regarding endometrial cancer risk. This study investigated the association between endometrial cancer risk and markers of insulin resistance, namely adiponectin, leptin, the A:L ratio, insulin, fasting glucose, and the HOMA-IR. We analyzed data from 541 incident endometrial cancer cases and 961 frequency age-matched controls in a population-based case–control study in Alberta, Canada from 2002 to 2006. Participants completed interview-administered questionnaires were assessed for anthropometric measures, and provided 8-h fasting blood samples either pre- or postoperatively. Blood was analyzed for concentrations of leptin, adiponectin, and insulin by immunoassay, and fasting plasma glucose levels were determined by fluorimetric quantitative determination. Compared with the lowest quartile, the highest quartile of insulin and HOMA-IR was associated with 64% (95% confidence intervals (CI): 1.12–2.40) and 72% (95% CI: 1.17–2.53) increased risks of endometrial cancer, respectively, and the highest quartile of adiponectin was associated with a 45% (95% CI: 0.37–0.80) decreased risk after multivariable adjustments. Null associations were observed between fasting glucose, leptin and A:L, and endometrial cancer risk. This population-based study provides evidence for a role of insulin resistance in endometrial cancer etiology and may provide one possible pathway whereby obesity increases the risk of this common cancer. Interventions aimed at decreasing both obesity and insulin resistance may decrease endometrial cancer risk.

Total fluid and specific beverage intake and risk of renal cell carcinoma in Canada.

BACKGROUND Intake of total fluids and specific beverages may be associated with the risk of renal cell carcinoma (RCC) through a diluting effect of carcinogens. However, total fluid consumption and RCC risk has not received sufficient examination. In this study, we assessed the roles of total fluid intake and type of beverage intake in the risk of RCC. METHODS Mailed questionnaires were completed by 1138 newly diagnosed, histologically confirmed RCC cases and 5039 population controls between 1994 and 1997 in 8 Canadian provinces. Data collection included information on socio-economic status, physical activity, smoking habits, alcoholic and non-alcoholic beverage use, diet, residential history and occupational history. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived through unconditional logistic regression. RESULTS Higher total fluid intake was associated with risk of RCC; the OR for the highest versus the lowest quartile was 1.49 (95% CI 1.20-1.85). Intake of total juices and coffee was also related to the risk of RCC; for the highest versus the lowest quartile, the ORs were 1.53 (95% CI 1.18-1.99) and 1.33 (95% CI 1.07-1.66), respectively. These positive associations were stronger in men, but not in women. Higher coffee intake was more strongly associated with RCC in normal weight subjects. In contrast, total intake of alcohol was inversely associated with the risk of RCC. Intake of tap water (not in coffee or tea), bottled water, tea, soft drinks and milk was not related to RCC. CONCLUSIONS The risk of RCC for higher intake of total fluids, coffee and juices might involve gender differences.

Case-control study of dietary patterns and endometrial cancer risk.

Dietary patterns, rather than intakes of specific foods or nutrients, may influence risk of endometrial cancer (EC). This population-based case-control study in Canada (2002–2006) included incident EC cases (n = 506) from the Alberta Cancer Registry and controls frequency age-matched to cases (n = 981). Past-year dietary patterns were defined using factor analysis of food frequency questionnaire data. Logistic regression was used to estimate EC risk within quartiles of dietary patterns. Three patterns (sweets, meat, plants) explained 23% of the variance in the dietary data. In multivariable models, EC risk was significantly reduced by 30% for women in the highest quartile of the healthier plants pattern (OR = 0.70, 95% CI 0.50–0.98, P trend = 0.02). When stratified by body mass index (BMI; kg/m2), risk was further reduced among overweight or obese women with a BMI ≥25 (OR = 0.57, 95% CI 0.39–0.83; P trend = 0.004). EC was not associated with the less healthy sweets and meat patterns. However, risk was modestly, but not significantly, elevated for higher intakes of the meat pattern among overweight or obese women. A mostly plant-based dietary pattern may reduce EC risk. Recommendations for risk reduction should focus on maintaining a healthy weight and the role of diet should be studied further.

Development and testing of a past year measure of sedentary behavior: the SIT-Q

BackgroundMost sedentary behavior measures focus on occupational or leisure-time sitting. Our aim was to develop a comprehensive measure of adult sedentary behavior and establish its measurement properties.MethodThe SIT-Q was developed through expert review (n = 7), cognitive interviewing (n = 11) and pilot testing (n = 34). A convenience sample of 82 adults from Calgary, Alberta, Canada, participated in the measurement property study. Test-retest reliability was assessed by intraclass correlation coefficients (ICCs) comparing two administrations of the SIT-Q conducted one month apart. Convergent validity was established using Spearman’s rho, by comparing the SIT-Q estimates of sedentary behaviour with values derived from a 7-Day Activity Diary.ResultsThe SIT-Q exhibited good face validity and acceptability during pilot testing. Within the measurement property study, the ICCs for test-retest reliability ranged from 0.31 for leisure-time computer use to 0.86 for occupational sitting. Total daily sitting demonstrated substantial correlation (ICC = 0.65, 95% CI: 0.49, 0.78). In terms of convergent validity, correlations varied from 0.19 for sitting during meals to 0.76 for occupational sitting. For total daily sitting, estimates derived from the SIT-Q and 7 Day Activity Diaries were moderately correlated (ρ = 0.53, p < 0.01).ConclusionThe SIT-Q has acceptable measurement properties for use in epidemiologic studies.

Case-control study of inflammatory markers and the risk of endometrial cancer.

Chronic inflammation may be important in endometrial cancer etiology. Several established endometrial cancer risk factors, particularly obesity, are hypothesized to operate through this pathway by increasing proinflammatory cytokines such as tumor necrosis factor &agr; (TNF-&agr;), interleukin-6 (IL-6), and acute-phase protein C-reactive protein (CRP). This study sought to investigate the association between inflammatory markers and the risk of endometrial cancer (types I and II). We recruited 519 incident endometrial cancer cases and 964 frequency age-matched controls in this population-based case–control study in Alberta (Canada) from 2002 to 2006. Participants completed in-person interviews, were assessed for anthropometric measures, and provided 8-h fasting blood samples either preoperatively or postoperatively. Blood was analyzed for the concentrations of TNF-&agr;, IL-6, and CRP by immunoassay. Endometrial cancer cases had consistently higher mean levels of TNF-&agr;, IL-6, and CRP compared with controls in these predominantly postmenopausal women. After adjusting for age, all markers were associated with statistically significant increased risks for endometrial cancer; however, after multivariable adjustment, only the risk from CRP remained elevated (odds ratio=1.22, 95% confidence interval: 1.02–1.47). Similarly, upon stratification by cancer type, only CRP was associated positively with an increased risk for type I endometrial cancer (odds ratio=1.25, 95% confidence interval: 1.03–1.52). All markers were associated with an elevated risk for the more rare and aggressive type II cancers; however, these findings were statistically nonsignificant, likely because of the small number of cases in this group. In conclusion, we found epidemiologic evidence for an association between CRP and the risk of endometrial cancer, which was slightly stronger for type I cancer. No associations emerged for TNF-&agr; and IL-6.

Risk of endometrial cancer in relation to individual nutrients from diet and supplements.

OBJECTIVE Intake of nutrients may influence the risk of endometrial cancer (EC). We aimed to estimate the association of intake of individual nutrients from food and from food plus supplements with EC occurrence. DESIGN A population-based case-control study conducted in Canada (2002-2006). SETTING Nutrient intakes from food and supplements were assessed using an FFQ. Logistic regression was used to estimate EC risk within quartile levels of nutrient intakes. SUBJECTS Incident EC cases (n 506) were identified from the Alberta Cancer Registry, and population controls were frequency- and age-matched to cases (n 981). RESULTS There existed little evidence of an association with EC for the majority of macronutrients and micronutrients examined. We observed a statistically significant increased risk associated with the highest, compared with the lowest, quartile of intake of dietary cholesterol (multivariable-adjusted OR = 1·51, 95 % CI 1·08, 2·11; P for trend = 0·02). Age-adjusted risk at the highest level of intake was significantly reduced for Ca from food sources (OR = 0·73, 95 % CI 0·54, 0·99) but was attenuated in the multivariable model (OR = 0·82, 95 % CI 0·59, 1·13). When intake from supplements was included in Ca intake, risk was significantly reduced by 28 % with higher Ca (multivariable-adjusted OR = 0·72, 95 % CI 0·51, 0·99, P for trend = 0·04). We also observed unexpected increased risks at limited levels of intakes of dietary soluble fibre, vitamin C, thiamin, vitamin B6 and lutein/zeaxanthin, with no evidence for linear trend. CONCLUSIONS The results of our study suggest a positive association between dietary cholesterol and EC risk and an inverse association with Ca intake from food sources and from food plus supplements.

Using national dietary intake data to evaluate and adapt the US Diet History Questionnaire: the stepwise tailoring of an FFQ for Canadian use.

OBJECTIVE To evaluate the Canadian Diet History Questionnaire I (C-DHQ I) food list and to adapt the US DHQ II for Canada using Canadian dietary survey data. DESIGN Twenty-four-hour dietary recalls reported by adults in a national Canadian survey were analysed to create a food list corresponding to C-DHQ I food questions. The percentage contribution of the food list to the total survey intake of seventeen nutrients was used as the criterion to evaluate the suitability of the C-DHQ I to capture food intake in Canadian populations. The data were also analysed to identify foods and to modify portion sizes for the C-DHQ II. SETTING The Canadian Community Health Survey (CCHS) - Cycle 2.2 Nutrition (2004). SUBJECTS Adults (n 20 159) who completed 24 h dietary recalls during in-person interviews. RESULTS Four thousand five hundred and thirty-three foods and recipes were grouped into 268 Food Groups, of which 212 corresponded to questions on the C-DHQ I. Nutrient intakes captured by the C-DHQ I ranged from 79 % for fat to 100 % for alcohol. For the new C-DHQ II, some food questions were retained from the original US DHQ II while others were added based on foods reported in CCHS and foods available on the Canadian market since 2004. Of 153 questions, 143 were associated with portion sizes of which fifty-three were modified from US values. Sex-specific nutrient profiles for the C-DHQ II nutrient database were derived using CCHS data. CONCLUSIONS The C-DHQ I and II are designed to optimize the capture of foods consumed by Canadian populations.